Amblyopia is a developmental visual disorder due to abnormal binocular input during an early critical period. It is characterized by low level deficis in acuity, contrast sensitivity, orientation discrimination, as well higher- level deficits in formand motion processing. Abnormalities have been found in V1 and V2, but fail to account for perceptual deficits implying further deficits must downstream. Our central hypothesis is that amblyopia stems from small deficits in early visual areas that are magnified downstream due to abnormal signal integration. To test this hypothesis, we will perform a series of behavior and physiology experiments to test both low and high level amblyopic deficits. We predict that amblyopic animals will be impaired on behavior tasks that require discrimination between global form stimuli. Neural responses to low-level grating stimuli will show deficits more severe than what has been reported in V1 and V2, more similar to perceptual deficits. Responses to high-level stimuli will exhibit shape selectivity, but to a more broad degree for amblyopic animals compared to visually normal controls. These experiments are critical to the overall understanding of the neural basis of amblyopia.